Contribution of systemic venous hypertension to the development of pulmonary edema in dogs.

Miller, Warner A.; Simi, Warren W.; Rice, David L.

doi:10.1161/01.res.43.4.598

Cited by 11 publications

(1 citation statement)

References 24 publications

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“…Such a small change would seem incapable of inducing pulmonary edema; thus redistribution of vascular resistance provides an unsatisfactory explanation of our data. The constancy of right ventricular end-diastolic pressure in the ligated group assured us that bronchial venous and pulmonary lymphatic hypertension were not responsible for the rise of PEV (Miller et al, 1978).…”

Section: Discussionmentioning

confidence: 85%

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Richeson¹,

Paulshock²,

Yun³

1982

Circulation Research

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SUMMARY Pulmonary edema which develops during acute myocardial infarction is generally believed to result solely from pulmonary microvascular hypertension. However, patients with myocardial infarction and pulmonary edema occasionally are found to have normal pulmonary wedge pressure. We report data indicating that pulmonary edema develops after coronary artery ligation despite stable microvascular pressure. Four groups of open-chest dogs were studied: (1) nine dogs with left anterior descending coronary artery ligation, (2) seven dogs with sham coronary ligation, (3) seven dogs ligated after beginning an infusion of indomethacin (5 mg/kg per hr), and (4) five dogs ligated after an infusion of the drug's vehicle was begun. Extra vascular lung water and pulmonary blood volume were measured at hourly intervals during the 2 hours before and after coronary ligation or sham ligation. Gravimetric lung water was measured immediately thereafter. Changes of net pulmonary intravascular driving force (the difference of microvascular hydrostatic and oncotic pressure) after ligation or sham ligation were small and comparable in all groups. Pulmonary blood volume did not change in any group. Pulmonary extravascular water volume remained constant in the sham group but rose significantly in the ligated group. Gravimetric lung water also was significantly higher in the latter group. We interpret these results to indicate that factors other than microvascular pressure can mediate the formation of edema during acute myocardial infarction; increased pulmonary microvascular permeability may be responsible. Indomethacin infusion blocked the formation of edema after coronary ligation, even though net microvascular driving force was highest in this group. Infusion of the vehicle alone did not prevent edema. The mechanism by which indomethacin exerts this protective effect is unclear but is probably a result of its inhibition of cyclo-oxygenase or cyclic nucleotide phosphodiesterase. Circ Res 50: 301-309, 1982PULMONARY edema is commonly categorized as "cardiogenic" or "non-cardiogenic," with the implication that the former type is mediated by pulmonary microvascular hypertension, whereas altered endothelial permeability accounts for the development of the latter form (Robin et al., 1972;Staub, 1974aStaub, , 1978. Pulmonary edema which develops in the setting of an acute myocardial infarction (MI) is generally believed to result solely from high pulmonary microvascular pressure, since depressed myocardial contractility, decreased left ventricular compliance, and peripheral venoconstriction commonly raise the pressure of the lesser circulation during acute MI. However, radiographic and clinical signs of pulmonary edema during MI are noted occasionally despite the presence of normal pulmonary wedge pressure (Nixon and Durth, 1968;Lassers et al., 1970; Kostuk et al., 1978;Timmis et

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Section: Discussionmentioning

confidence: 85%

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Richeson¹,

Paulshock²,

Yun³

1982

Circulation Research

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Thoracic duct lymph and PEEP studies in anaesthetized dogs

Haider¹,

Schad

Mendler

1987

Intensive Care Med

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The effect of positive end-expiratory pressure ventilation (PEEP, 11-12 mmHg, 60-90 min without, 19 h with circulatory support) on fractional escape rate of plasma proteins (FER), and on thoracic duct lymph flow draining against jugular venous (LFJVP) or atmospheric pressure (LFAP) was studied in anaesthetized dogs. FER was 10.8%/h, 15.3%/h, and 8.5%/h before, during, and after PEEP, respectively, indicating augmented lymph formation probably due to the increase in venous pressure from 4.8 to 10.8 mmHg during PEEP. LFJVP was 39 microliter/min per kg before PEEP, decreased transiently during PEEP but the steady state value (up to 19 h) was not different from control, and increased transiently after PEEP. LFAP was 37, 80, and 38 microliter/min per kg before, during, and after PEEP, respectively. Long-term PEEP increased LFAP fourfold. Changing the drainage mode during PEEP yielded an immediate increase from LFJVP = 34 to LFAP = 79 microliter/min per kg and an instantaneous reduction from LFAP = 95 to LFJVP = 35 microliter/min per kg. Lymph protein concentration and protein lymph/plasma ratio increased concomitantly with LFAP during PEEP suggesting augmented hepatic contribution to LFAP, augmented intestinal contribution was revealed by labelling intestinal lymph using olive oil orally, muscular lymph flow was not increased as shown by i.m. Evans blue. In conclusion, the augmentation of venous pressure by PEEP promotes capillary filtration but obstructs lymph drainage from the thoracic duct into the jugular vein. PEEP imbalances formation and return of lymph and affects the development and removal of oedema.

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Thoracic duct lymph and PEEP studies in anaesthetized dogs

1987

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PEEP impedes thoracic duct drainage (LF). This can be counteracted by a thoracic duct fistula. Consequently, lung oedema (LOE) should develop during PEEP more slowly with LF at atmospheric pressure (LFAP) than with LF against jugular venous pressure (LFJVP). In 12 anaesthetized dogs LOE was produced by Ringer's solution i.v. (2.5 ml/min per kg) for 6 h during PEEP (10 mmHg) with either LFAP or LFJVP. Ringer's + PEEP greatly increased aortic, pulmonary artery and wedge pressures, JVP, and cardiac output. Colloid osmotic pressures in plasma and lymph were drastically reduced, pulmonary effective filtration pressure (EFP) rose by about 20 mmHg. LFJVP increased 7-fold, LFAP about 19-fold, the respective loss of plasma proteins was 1.83 and 1.06 g/kg during 6 h. Thermal-dye extravascular lung water showed an increment of 68 with LFJVP versus 43 microliter/h/g per mmHg with LFAP. Final lung water content was at any delta EFP (12.8-31.9 mmHg) lower with LFAP than with LFJVP amounting 512 with LFJVP versus 377 microliters/g/per mmHg with LFAP. LFAP decreased the development of LOE during PEEP by bypassing the PEEP-induced high JVP and thus facilitating the removal of interstitial fluid. It is hypothesized that a thoracic duct fistula might aid the treatment of patients with LOE due to ARDS and therefore requiring high levels of PEEP.

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Contribution of systemic venous hypertension to the development of pulmonary edema in dogs.

Cited by 11 publications

References 24 publications

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Non-hydrostatic pulmonary edema after coronary artery ligation in dogs. Protective effect of indomethacin.

Thoracic duct lymph and PEEP studies in anaesthetized dogs

Thoracic duct lymph and PEEP studies in anaesthetized dogs

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